Changes of NGFI-B subcellular location in cardiomyocytes of stressed rats and its biological effects / 中国应用生理学杂志
Chinese Journal of Applied Physiology
;
(6): 289-293, 2011.
Article
in Chinese
| WPRIM
| ID: wpr-351174
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the changes of expression and subcellular location of nuclear growth-induced protein-B(NGFI-B) in cardiomyocytes of stressed rats and its biological effect and to provide scientific evidences for exploring the mechanism underlying myocardium injury induced by stress.</p><p><b>METHODS</b>The cell model of stress-induced cardiomyocyte injury were established. Western blot method and confocal microscopy method were used to investigate the subcellular location of NGFI-B in cardiomyocytes under stress. The flow-cytometry was selected to detect the apoptotic rate in cardiomyocytes in vitro. Western blot method was used to determine the content of cytochrome C protein in mitochondria and cytoplasm respectively.</p><p><b>RESULTS</b>Stress induced the increase of NGFI-B content in the mitochondria of cardiomyocytes and the translocation of NGFI-B from the nucleus to the mitochondria. The translocation of NGFI-B promoted the release of cytochrome C from the mitochondria and the cardiomyocyte apoptosis. Treatment of stressed cardiomyocytes with leptomycin B, a non-specific blocker of nuclear export, resulted in nuclear retention of NGFI-B and abrogated its ability to induce the release of cytochrome C from the mitochondria.</p><p><b>CONCLUSION</b>Stress could induce NGFI-B translocation from the nucleus to the mitochondria in cardiomyocytes, which activated the mitochondrial pathway of cell apoptosis.</p>
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Stress, Physiological
/
Cells, Cultured
/
Rats, Wistar
/
Apoptosis
/
Cell Biology
/
Myocytes, Cardiac
/
Nuclear Receptor Subfamily 4, Group A, Member 1
/
Animals, Newborn
/
Metabolism
Type of study:
Prognostic study
Limits:
Animals
Language:
Chinese
Journal:
Chinese Journal of Applied Physiology
Year:
2011
Type:
Article
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